The dominance of the coronary arterial system was determined angiographically in 75 adult patients with isolated aortic stenosis with or without insufficiency, 25 adult patients with pure aortic insufficiency, 51 adult patients with combined aortic stenosis and mitral valve disease, and 44 children with bicuspid aortic valves. There was an unusually high incidence of left dominance in adults with isolated aortic stenosis (36%) and in children with bicuspid aortic valves (56.8%). These findings suggest the existence of a variant developmental complex consisting of a bicuspid aortic valve and reversal of dominance of the coronary arterial system. Furthermore, it adds support to the concept that progressive stenosis of a bicuspid aortic valve is frequently the etiology of isolated aortic stenosis in adults.
SUMMARY The anatomy of the proximal left coronary artery in 33 adult patients with bicuspid aortic valves was compared with that in 33 adult patients with aortic valve disease ofother aetiologies and with that in 50 adult control patients with no valve or congenital heart disease. Patients with bicuspid aortic valves had a higher incidence of immediate bifurcation of the left main coronary artery, of left main coronary length less than 10 mm, and of left cdrouary artery dominance. The mean length of the left main coronary artery was significantly less in the patients with bicuspid aortic valves. These variations from the usual coronary artery anatomy may be part of the developmental abnormalities responsible for bicuspid aortic valves, and require evaluation and consideration when considering angiography and valve replacement in patients with aortic stenosis.Aortic stenosis occurring in the setting of a congenitally abnormal aortic valve has been associated with several other congenital abnormalities, including coarctation of the aorta, hypoplastic left heart syndrome, and reversal of dominance of the coronary arterial system (Reifenstein et al., 1947;Becker et al., 1970;Simon and Reis, 1971;Rosenquist, 1974;Higgins and Wexler, 1975 MethodsWe reviewed the cardiac catheterisation data, cineangiograms, and coronary angiograms of the most recent 100 consecutive adult patients studied in our institutions who had clinical, haemodynamic, and angiographic evidence of aortic valve disease. In 66 of these patients, the anatomy of the aortic valve could be determined with certainty, and selective coronary angiograms were of adequate quality to evaluate the origin and length of the left main coronary artery. The most recent 50 patients with no clinical or haemodynamic evidence for valvular or congenital heart disease who underwent coronary angiography and -cardiac catheterisation served as a control group.Coronary angiograms were obtained in multiple projections using 6 in Philips caesium iodide image intensifiers and 35 mm Arriflex cameras. The length of the left main coronary artery was measured in that projection (usually between 10 and 45 degrees right anterior oblique), where the left main coronary artery was judged to be perpendicular to the x-ray beam and where the site of bifurcation of the left anterior descending and circumflex coronary arteries could be most objectively identified (Fig. 1)
Significant sex differences in the correlation of electrocardiographic exercise testing and coronary arteriograms. Am J Cardiol 36: 169, 1975 40. Cumming GR, Dufresne C, Kich L, Samm J: Exercise electrocardiographic patterns in normal women. Br Heart J 35: 1055Heart J 35: , 1973 41. Linhart JW, Laws In the presence of systemic hypocalcemia the myocardial depressant actions of this contrast material were accentuated.Intracoronary administration of contrast material with added Ca+-, calcium sodium meglumine metrizoate, caused no myocardial depression. Total calcium decreased only slightly (10.2 ± 0.2 to 9.1 ± 0.2 mg%), while Ca-t increased (4.8 ± 0.1 to 5.1 ± 0.2 mg%). During systemic hypocalcemia, the calcium metrizoate compound induced increases in LVPSP and dp/dt/LVP40. Thus, contrast materials caused myocardial depression which, at least in part, was related to reductions of ambient calcium through a dilutional and binding action. The addition of Ca-to monomeric contrast materials reversed the myocardial depressant action and produced a transient rise in ambient Ca-. ACUTE LEFT VENTRICULAR power failure and electromechanical dissociation are rare but disastrous complications of coronary arteriography. Currentlyutilized ionic contrast materials have a direct depressing action on the ventricular myocardium which is related at least in part to the hyperosmolarity1 and high sodium ion content4 I of the solution. This solution, which displaces blood during coronary arteriography, is also deficient in calcium ions (Ca++), which have a critical role in contraction of the sarcomere.6-10 Moreover, it has been suggested that the material most frequently used for coronary arteriography contains chelating properties which might further reduce ambient Ca++ in the myocardium.1' It is wellestablished from early investigations6 9 that excitation-contraction coupling depends on the presence of free Ca++, and electromechanical dissociation ensues upon lowering ambient Ca+-in perfusate of isolated heart preparations. Recently, contrast material has been implicated as a causative factor in electromechanical dissociation occurring during coronary arteriography." The purpose of this study was: 1) to determine the extent of and the mechanism by which calcium is lowered in the coronary circulation during coronary arteriography; 2) to compare the severity and time sequence of depression in calcium levels in a "control state" and an induced acute heart failure state; 3) to assess the influence of preexisting systemic hypocalcemia on the myocardial depression induced by contrast materials; and 4) to compare the effects on calcium levels and myocardial contractility of a contrast material containing calcium ions with currently used non-calcium-containing contrast materials. Methods
Fifty-one patients were divided into two groups: 20 patients with proven rheumatic mitral valve disease (RMVD) and 31 patients with left atrial enlargement (LAE) of a nonrheumatic etiology. The latter group included patients with ischemic papillary muscle dysfunction, mitral valve prolapse, and congestive cardiomyopathy. Radiographic studies showed that enlargement of the left atrial appendage (LAAE) was present in 18 of 20 rheumatics but in only one of 31 non-rheumatics. There was no direct relationship between enlargement of the LAA and radiographic or echocardiographic left atrial size, degree of pulmonary venous hypertension (PVH), or presence of atrial fibrillation. It is postulated that rheumatic inflammation of the LAA allows it to dilate out of proportion to the body of the left atrium. In the adult patient with radiographic findings of PVH, LAAE is a valuable and specific radiographic sign of rheumatic mitral valve disease.
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